Post Graduate Diploma in EMERGENCY

MEDICAL SERVICES (PGDEMS)

HUB: Life Supporters Institute of Health Sciences
University: Tata Institute of Social Sciences

Project By
Dr.Chaitali choraghe

Under Guidance
of Dr.Paresh
Navalkar

1|Page
CASE STUDY :- UNSTABLE ANGAINA

Tata Institute of social science

School Vocation Education

PGDEMS

2|Page
TABLE OF CONTENT

 Abstract
 Introduction
 Literature view
 Case presentation
 Management and outcome
 Discussion
 Current research/study
 Upcoming research/study
 Acknowledgement
 References

3|Page
 ABSTRACT
Unstable angina is one of the most common reasons for hospital
admission in the United States and causes substantial morbidity and
mortality.. Diagnosis of unstable angina is complicated by the dynamic
range of presentations, which can vary between atypical chest pain . In
this we see brief about unstable angina and its management.
Overcautious management can result in unnecessary hospital
admission, whereas inappropriate conservative strategies can cause
cardiac injury and death. To define treatment strategies for these
patients, the US Agency for Health Care Policy and Re search in March
1994 published guidelines on the diagnosis and management
of unstable angina. The emphasis is on diagnosis or exclusion of
coronary artery disease, establishment of the patient's risk for adverse
outcome, and triage to the most appropriate treatment regimen. The
guidelines emphasize the use of aspirin, heparin sodium, and beta-
blockers as the core therapy. Appropriate strategies are reviewed,
starting with intensive medical management and ending with patient care
after discharge.

Keywords:-

Acute coronary syndrome ,cardiac rehabilitation ,chronic stable angina

Aspirin, Heparin, Unstable Angina, Myocardial Infarction,Direct
Thrombin Inhibitor, low molecular weight

4|Page
 INTRUDUCTION
Unstable angina or sometimes referred causes unexpected
chest pain and usually occurs while resting. The most common
cause is reduced blood flow to the heart muscle because the
coronary arteries are narrowed by fatty build-ups
(atherosclerosis ) which can ruptured causing injury to the
coronary blood vessel resulting in blood clotting which blocks
the flows of blood to the heart muscles.
Unstable angina should be treated as an emergency. if you
have new ,worsening or persistent chest discomfort ,you need
to go to the ER. you could be having a heart attack which puts
you at increased risk for severe cardiac arrhythmias or cardiac
arrest ,which could lead to sudden death .

Causes:-
Blood clots that block an artery partially or totally are what
causes unstable angina .Blood clots may form, partially
dissolve and later form again and angina can occur each time a
clot blocks blood flow in an artery .

Symtoms :-
The pain or discomfort
 Often occurs while you may be resting, sleeping or
with little physical exertion.
 Squeezing ,Heaviness, Tightening
 Burning or aching across the chest, usually starting
behind the breastbone.
 This pain often spreads to the neck, jaw, arms
shoulders, throat, back or even the teeth.
Patient also complaint of symptoms including :-

5|Page
 Indigestion
 Heartburn
 Weakness
 Nausea
 Cramping shortness of breath
 Rest or medicine usually do not help relive it
 May get worse over time
 Can lead to a heart attack

 Pathogenic mechanisms in
unstable angina
 In the mid-1980s, several researchers10-
12
suggested that unstable angina was
linked to non–Q and Q wave MI, and that
these conditions represented a spectrum
of disease in which plaque disruption or
fissuring led to thrombus formation and
the acute coronary syndrome.
Intracoronary thrombus formation was
thought to explain the pathogenesis in
most patients with unstable angina. As
opposed to MI with ST-segment elevation
in which the thrombus was usually
occlusive, the thrombus in unstable angina
was mural and did not result in total
coronary occlusion in 80% to 90% of
patients (Figure 1).13 Non–Q wave infarction
is positioned between the other 2
conditions because there was more
frequent total occlusion of the culprit
artery than in unstable angina but less
than in Q wave MI.14,15

6|Page
 Nearly all pathologic evidence in acute
syndromes originates from autopsy
studies.16Because short-term mortality of
unstable angina is low, autopsy data in
unstable angina represent a highly select
population. Aside from these, pathologic
material in unstable angina has been
obtained mainly from atheromatous plaque
that is excised during directional
atherectomy of the culprit lesion. 17,18 This
analysis is subject to sampling error
because only a portion of the plaque is
removed. Accordingly, our understanding of
its pathogenesis derives mainly through
other methods, including angiography,
angioscopy, and biochemical studies.

 Thrombus Formation in Unstable Angina

 Results of angiographic
10,19,20
studies suggest that intracoronary
thrombus formation or a complex lesion
(ulcerated or irregular plaque) is found in
50% to 80% of culprit lesions, particularly
if the presentation is rest pain. Serial
angiograms performed before and after an
episode of unstable angina, without an
intervening coronary intervention, have
shown progression of coronary artery
disease in about 75% of patients.21,22

 Recently, Dangas et al23 correlated

coronary morphologic features of the
culprit lesion to the Braunwald
7|Page
classification. There were significant
(P<.05) positive correlations between
severity of the unstable angina
presentation and presence of an
intracoronary thrombus or complex lesion.
Results of angioscopic studies24 also
indicate that intracoronary thrombus or
yellow plaque is found in most unstable
culprit arteries but infrequently in stable
angina. The thrombus in unstable angina
has been characterized as grayish-white
and presumably platelet-rich, whereas in
MI it was red.25 Because the coronary
artery is usually totally occluded in MI,
this red thrombus is rich in fibrin and red
blood cells, superimposed on the platelet
component and potentiated by stasis of
blood flow. Although angiography is
commonly used to detect thrombus, it has
low sensitivity relative to
angioscopy.26,27However, angiography is
relatively specific (80%-90%) for the
detection of thrombus or a complex
lesion.26,27 Small thrombi or mural thrombi
that do not cause luminal irregularity
probably cannot be detected
angiographically. In conclusion, thrombus
formation on a presumed disrupted,
fissured, or eroded plaque is the most
common pathophysiological mechanism in
unstable angina, particularly when the
presentation is that of acute rest pain.

8|Page
 However, it is unrealistic to assume that
thrombus formation can explain all
unstable presentations. For patients
without rest pain, there are less
convincing data that thrombus is the
predominant cause. In our opinion, these
patients require further evaluation.

 Other Pathogenic Mechanisms in Unstable

Angina
 Other mechanisms might explain the
clinical syndromes of unstable angina.
Inflammation has been implicated.
Inflammation plays a role in plaque
rupture, contributing to destabilization of
the fibrous cap of so-called vulnerable
plaques by the secretion of matrix
metalloproteinases.28 Results of directional
atherectomy analysis of culprit lesions in
unstable angina show a higher percentage
of the excised plaque area infiltrated by
inflammatory cells compared with stable
angina. One difficulty with understanding
the role of inflammation is the
interrelationship between thrombus
formation and inflammation. Tissue factor
is found more commonly in unstable vs
stable plaques, and results of
histopathologic analysis29,30 of atherectomy
specimens show a strong association
between macrophage infiltration and
tissue factor localization. Local expression
of tissue factor by macrophages can lead
9|Page
 to activation of the coagulation cascade.
Furthermore, activation of platelets might
lead to inflammatory reactions at the site
of vascular lesions.31 Another link between
inflammation and thrombosis might be
lipoprotein(a). Recent data32 suggest that
lipoprotein(a), which is considered
atherosclerotic and thrombogenic, also
colocalizes in macrophage-rich areas in
unstable plaques. At the molecular level,
the apolipoprotein A portion of the
lipoprotein(a) molecule has been
33
shown to be responsible for macrophage
chemoattraction.

 Another potential nonthrombotic

mechanism for unstable angina might be
smooth muscle cell proliferation. In lesions
without angiographic evidence of
thrombus, some patients have an abundant
proliferation of smooth muscle cells on
directional atherectomy analysis of
excised plaque similar to that found in
restenotic lesions.34 Again, excluding a role
for thrombus is difficult because one third
of lesions had thrombus demonstrated on
tissue analysis, although the angiogram
suggested no thrombus. Furthermore,
thrombus might be a potent stimulus for
smooth muscle cell proliferation, along
with cytokines or growth factors released
from inflammatory cells or other stimuli,
including infectious agents like Chlamydia
10 | P a g e
 pneumoniae and
cytomegalovirus.35 Smooth muscle cell
proliferation without thrombus might play
a role in unstable angina in the restenotic
lesion. Restenotic lesions do not usually
contain thrombus, yet their presentation
might be that of rest pain even with
enzyme level elevation, indicating non–Q
wave MI (Figure 2).

 Finally, occasionally there are patients

who present with rest ischemia and ST-
segment elevation in whom vasospasm on
an angiographically normal-appearing
vessel is present. However, most patients
with so-called Prinzmetal variant angina
have fixed and severe atherosclerotic
lesions with superimposed thrombus.

 Pathogenic vs Ischemic Mechanisms in

Unstable Angina
 In general, the pathogenesis of coronary
disease relates to the slow or rapid
progression of atherosclerosis. Ischemic
mechanisms, on the other hand, reflect an
imbalance between myocardial blood
supply and oxygen demand. As physicians,
we evaluate patients with silent or clinical
ischemia. In unstable angina, transient
decreases in blood supply or even small
increases in myocardial demand in the
presence of a new significant lesion might
precipitate ischemic manifestations of the
11 | P a g e
 disease, namely, angina, by altering this
balance. Transient decreases in supply
related to intracoronary thrombus
formation with spontaneous lysis or
embolization, or transient increases in
vasomotor tone, might lead to rest pain.
Activated platelets release several
vasoactive substances that, in the
presence of endothelial dysfunction
(impaired vasodilation), can result in
vasoconstriction at or distal to the lesion
and a transient decrease in blood flow.
Although a thrombus is usually present to
explain or contribute to decreases in blood
supply, any process (thrombotic or
otherwise) that significantly perturbs this
balance can lead to unstable angina.

TREATMENT FOR UNSTABLE ANGINA:-

First ,your healthcare provider will need to find the blocked
part or parties of the coronary arteries by performing a

12 | P a g e
cardiac catheterization. In this procedure a catheter is
guided through an artery in the arm or leg and into the
coronary arteries, then injected with a liquid dye through
the catheter. High speed x-ray movies record the course of
the dye as it flows through the arteries, and doctors can
identified blockage by tracing the flow. An evaluation of
how well your heart is working also can be done during
cardiac catheterisation Next, based on the extent of the
coronary artery blockage your doctors will discuss with
you the following treatment options

1)Percutaneous coronary
intervention(PCI):-
May be required to open a blockage coronary artery.
Briefly, this procedure involves undergoing cardiac
catheterisation following by using a catheter with a small
inflatable balloon at the tip .The balloon is inflated,
squeezing open the fatty plaque deposit located on the
inner lining of the coronary artery .
Then the balloon is deflated and the catheter is withdrawn.
This procedure is often followed by insertion of a stent to
then keep the coronary artery vessel propped open to
allow for improved blood flow to the heart muscles
2) coronary artery bypass graft surgery may be
indicated depending on the extent of coronary artery
blockage and medical history .in this procedure ,a blood
vessel is used to route blood around the blockade part
of the artery, forming a kind of detour.
Before any of these procedure a doctor must find the
blockage part or parts of the coronary arteries. He or she
will guide a catheter through an artery in term or leg and
13 | P a g e
into the coronary arteries, then inject a liquid dye through
the catheter. High speed x-ray movies record the course of
the dye as it flows through the arteries and doctor can
identify blockages by tracing the flow .An evaluation of
how the heart works also can be done during cardiac
catheterisation.

Case presentation
This is a case of 50yrs old male patient presented with
complaint of left sided chest pain and palpitation.

Patient had left sided chest pain in the morning but after
taking rest he felt better, But on the same day in the
14 | P a g e
 afternoon he had again the same episode of chest pain
which is not relieved by rest.

Patient told that he felt heaviness on the left sided of chest

radiating towards the left shoulder and had mild difficulty in
breathing , so releatives brought the patient in the
emergency room .

Patient was known case of hypertension since 3years ago

but 1 years ago he had not taken any medicine .

In the past history had same episode of the chest pain in

2008,but at the time doctors told that ECG was normal .

Personal habit the patient was chronic tobacco chewer

years and had taking alcohol occasionally

Patient did not have any major illness in the family history.

Patient was operated for Appendectomy before 2years

back When patient was brought to casuality,patient was
conscious and well oriented

ON General examination

Temperture:-98.6F

Pulse -76b/min

BP-150/90mmHg,

RR-16b/min
15 | P a g e
,spo2-95%

,HGT-148mg/dl.

Systemic examination:-

CVS:-S1 &S2 heard

CNS:-conscious and well oriended

RS:- AEBE

GI:-soft

Management

Patient came to the emergency department, patient

saturation was 95% so addministerd nasal cannula at 2lit
of O2 and spo2 maintained 98%.

The ECG was done and Blood investigation was sent to

lab (CBC, RFT , LFT ,Sr electrolyte , PT /INR, CPK-MB ,
Trop – I , HHH),send to lab

And in ECG shown T wave inversion in v1-v4

16 | P a g e
Due to ischemic changes, Tablet ecosprin 300mg ,Tablet
clopitab 300mg ,Tab Atorva 80mg was given on stat ,and
also inj pan 40mg , inj Emset 4mg /IV was given in
emergency department

Then patient was shifted to ICU and unstable angina

under evaluation ,In ICU department, seen cardiologist
,and patient advice for chest x-ray , 2D ECHO ,Lipid profile
,and plan for CAG and then cardiologologist start
treatment

Inj monocef 1gm IV (1-0-1)

Inj PAN 40mg Iv (1-0-1)

Inj Emset 40mg (1-0-1)

Inj HEPARIN 4000IU 6hrly

Tab ecosprin 150mg-(0-1-0) ,

Tab Atorva 80mg-(0-0-1)

Syp sucralfate 10ml(1-1-1)

As the x-ray,2DEcho and blood investigation report was

normal and also cardiac enzymes, Trop –T negative and
CPK-MB normal

As Trop-T negative and CPK-MB normal so patient

diagnosed as unstable angina.

17 | P a g e
 Blood Investigation Report

Haematology PT Test 14.6

INR 1.19

Cardiac Enzymes Trop T Negative

CKMB 24
RFT BUN 11

Sr.Creat 0.8
LFT Total Bilirubin 1.2
SGOT 25

SGPT 25
Sr. Electrolytes NA+ 140
K+ 4.8

Cl 101

Lipid Profile LDL 158 18 | P a g e

HDL 60

Total Cholesterol 239

19 | P a g e
20 | P a g e
21 | P a g e
22 | P a g e
23 | P a g e
LEGENDS

CARDIAC ENZYMES / CARDIAC BIOMARKERS

Cardiac enzymes ― also known as cardiac biomarkers ―

include myoglobin, troponin and creatine kinase. Historically,
lactate dehydrogenase, or LDH, was also used but is non-specific.
Cardiac enzymes are released into the circulation when myocardial
necrosis occurs, as seen in myocardial infarction.

MYOGLOBIN

Myoglobin is released into circulation with any damage to

muscle tissue, including myocardial necrosis. Because skeletal
muscle contains myoglobin, this measurement is quite nonspecific
for MIs. The benefit in myoglobin is that a detectable increase is
seen only 30 minutes after injury occurs, unlike in troponin and
creatine kinase, which can take between 3 and 4 hours.

TROPONIN

The enzymes troponin I and troponin T are normal proteins that

are important in the contractile apparatus of the cardiac
myocyte. The proteins are released into the circulation between
3 and 4 hours after myocardial infarction and remain detectable
for 10 days following. This long half- life allows for the late
diagnosis of MI but makes it difficult to detect re-infarction, as
can occur in acute stent thrombosis after percutaneous coronary
intervention, or PCI. There are a number causes for troponin
elevation not related to myocardial infarction; however, troponin
elevation is much more sensitive than myoglobin and even

24 | P a g e
 creatine kinase.

CREATINE KINASE (CK)

Creatine kinase ― also known as creatine phosphokinase, or CPK

― is a muscle enzyme that exists as isoenzymes. The MB type is
specific to myocardial cells, whereas MM and BB are specific to
skeletal muscle and brain tissue, respectively. The CK level
increases approximately 3 to 4 hours after MI and remains
elevated for 3 to 4 days. This makes it useful for detecting re-
infarction in the window of 4 to 10 days after the initial insult;
troponin remains elevated for 10 days, making it less useful for
this purpose.

Differential Diagnosis UNSTABLE ANGINA:-

Disease/Condition Differentiating Signs/Symptoms Differentiating Tests

Stable angina Pain occurs only in context of exertion ECG may be normal in the absence
or emotional stress, not worsening over of pain but may show ST
time, and relieved by nitrates or rest. depression during episodes of
angina or on stress testing.

Prinzmetal (variant Typically occurs without provocation ST elevation during acute

or vasospastic) and usually resolves spontaneously or episode. [3]
angina with rapid-acting nitrate. [3] Coronary angiography (invasive or
May be precipitated by emotional noninvasive) excludes severe
stress, hyperventilation, exercise, or a obstructive coronary artery disease
cold environment. [3] [47] but may show spasm. [3] (Fixed
Most episodes occur early in the lesions and spasm may coexist.)

25 | P a g e
Disease/Condition Differentiating Signs/Symptoms Differentiating Tests

morning. [3] Nonpharmacologic provocative

May be younger and/or smoker. [3]
Calcium-channel blockers suppress
symptoms (beta-blockers do not
suppress symptoms). [47]
tests (e.g., cold pressor or
hyperventilation) or pharmacologic
(e.g., acetylcholine) under
supervision and in absence of
contraindications to provocative
testing (left main disease, advanced
3-vessel disease, presence of high-
grade obstructive lesions, significant
left-ventricular systolic dysfunction,
advanced heart failure) may be
diagnostic when invasive
assessment is not helpful. [3]

Non-ST-elevation Clinical presentation may be ECG may be normal or show ST

myocardial infarction indistinguishable. depression or T wave inversion.
Cardiac biomarkers (troponin,
creatine kinase [CK], CK-MB) are
elevated.

ST-elevation Clinical presentation may be ECG shows persistent ST elevation

myocardial infarction indistinguishable. in 2 or more leads. Cardiac
biomarkers (troponin, creatine
kinase [CK], CK-MB) are elevated.

Congestive heart Breathlessness, orthopnea, Echocardiogram shows reduced left

failure tachycardia, and peripheral edema are ventricular ejection fraction or signs
usually predominant. Chest pain may of diastolic dysfunction.
occur if coronary perfusion is poor.
CXR may show congestion,
cardiomegaly, or pleural effusion.
B-type natriuretic peptide: elevated.

Chest wall pain Onset often insidious, and may be
history of repetitive movement or minor
trauma. Pain may be reproduced on
palpation or movement. Not improved
with rest or nitrates but may be relieved
by local injection of lidocaine.
CXR or bone scan may show
skeletal pathology such as rib
fracture, osteoarthritis, or metastatic
tumor. Diagnosis of soft tissue
lesions is clinical.

Pericarditis Recent myocardial infarction, renal ECG: concave ST elevation in all

failure, chest irradiation, or associated leads except aVR; PR segment
connective tissue disease. depression.
Pain relieved by sitting up and leaning Echo: may show minimal pericardial
forward and is worse when lying effusion, but is frequently normal.

26 | P a g e
Disease/Condition Differentiating Signs/Symptoms Differentiating Tests

supine. If pleuropericarditis, the pain

may be worse or present only on
inspiration.
Pericardial rub may be heard.

Myocarditis May be preceded by viral infection. ECG may show evidence of

pericarditis or myopericarditis (ST
Symptoms of myocarditis include chest
elevation or nonspecific ST-T
pain (which may be pleuritic as a result
changes). Other findings include
of concomitant pericarditis),
arrhythmias or conduction
palpitations, fatigue, or signs of heart
disturbances.
failure (e.g., peripheral edema,
increasing dyspnea, and weight gain). Echocardiogram is helpful in
excluding other causes of heart
failure (e.g., valvular heart disease).
Troponin levels are elevated in up to
one third of cases.
Serum viral antibody titers may
suggest recent viral infection, but
testing is rarely indicated in the
diagnosis of viral myocarditis or any
dilated cardiomyopathy, owing to its
low specificity and the delay of
rising viral titers, which would have
no impact on therapeutic decisions.
Antimyosin scanning helps in
diagnosis and when compared with
endomyocardial biopsy shows a
sensitivity of 83% and a specificity
of 53%.
MRI shows an area of delayed
hyper-enhancement that does not
match a coronary artery territory.
Endomyocardial biopsy is
necessary to establish a confirmed
diagnosis of myocarditis. Histologic
criteria for myocarditis are well
established. [48]However, routine
biopsy for establishing diagnosis of
myocarditis is rarely helpful
clinically, because histologic
diagnosis seldom has an impact on
therapeutic strategies, unless giant
cell myocarditis is suspected.

27 | P a g e
Disease/Condition Differentiating Signs/Symptoms Differentiating Tests

Aortic dissection History of hypertension, or Marfan or CXR: may show wide mediastinum.
Ehlers-Danlos syndrome. Occasionally
CT chest or transesophageal echo:
precipitated by pregnancy.
visualization of luminal flap will
Severe tearing chest pain radiating confirm the dissection.
between shoulder blades.
Unequal pulses, interarm differential
blood pressure, diastolic murmur of
aortic regurgitation.

Pulmonary Recent surgery, immobilization, ECG: sinus tachycardia, right

embolism prolonged air travel, or cancer.
Acute shortness of breath, pleuritic
chest pain, or syncope.
Hypoxia, cyanosis, elevated jugular
venous pressure with hypotension and
clear lung fields.
bundle branch block, S1Q3T3
pattern.
CXR: oligemic and hyperlucent lung
fields, wedge-shaped infarct if
pulmonary infarction.
V/Q scan: pulmonary embolism is
likely when an area of ventilation is
not perfused.
CT angiogram: reveals pulmonary
embolism/thrombus.

Pleuritis Recent viral infection or prodrome of CXR: may show resolving

infection. pneumonia.
Chest pain worse with inspiration.
Audible pleuritic rub.

Pneumothorax Underlying lung disease, trauma, or CXR: collapsed lung.

recent procedures (such as insertion of
central venous line).
Acute chest pain with shortness of
breath.
If large, will lead to tracheal deviation,
hyper-resonance, and decreased air
entry.

Perforated History of previous peptic ulcer Erect CXR and abdominal series:
abdominal viscus disease, diverticulitis, or recent bowel gas under the diaphragm.
biopsy.
CT abdomen: confirm the presence
Typically presents with abdominal pain. of free gas within the abdomen and
Chest pain is referred but may be peritoneal cavity.
mistaken for cardiac origin.

28 | P a g e
Disease/Condition Differentiating Signs/Symptoms Differentiating Tests

Abdominal examination shows

localized tenderness and, in cases of
peritonitis, generalized tenderness.

DISCUSSION

29 | P a g e
IN This case, patient came with chest pain and ECG
show lead V1 to V5 T inversion,so there will be ischemic
changes in anterio-lateralportion of heart.patient
provisionally diagnosed as unstable angina under
evaluation.as the cardiac enzymes (Trop-
T,CPKMB)negative ,so patient diagnosed as unstable
angina /antiplatelates, anti –coagulant, statin and beta-
blockers are given ,,in this case ,we can also use
glycoprotein iib /iiia inhibitors to prevent further blocking
of coronary artery and to restore the perfusion of
myocardia .

30 | P a g e
Current research/study
OBJECTIVES: To describe common barriers that limit the effect of
guidelines on patient care, with emphasis on recommendations for triage
in the Agency for Health Care Policy and Research (AHCPR) Unstable
Angina Clinical Practice Guideline. DATA SOURCES: Previously
reported results from a prospective clinical study of 10,785 patients
presenting to the emergency department (ED) with symptoms
suggestive of acute cardiac ischemia. STUDY DESIGN: Design is an
analysis of the AHCPR guideline with regard to recognized barriers in
guideline implementation. Presentation of hypothetical scenarios to ED
physicians was used to determine interrater reliability in applying the
guideline to assess risk and to make triage decisions. PRINCIPAL
FINDINGS: The AHCPR guideline's triage recommendations
demonstrate (1) poor interobserver reliability in interpretation by ED
physicians; (2) limited applicability of recommendations for outpatient
management (applies to 6 percent of patients presenting to the ED with
unstable angina); (3) incomplete specifications of exceptions that may
require deviation from guideline recommendations; (4) unexpected
effects on medical care by significantly increasing the demand for limited
intensive care beds; and (5) unknown effects on patient outcomes. In
addition, analysis of the guideline highlights the need to address
organizational barriers, such as administrative policies that conflict with
guideline recommendations and the need to adapt the guideline to
conform to local systems of care. CONCLUSIONS: Careful analysis of
guideline attributes, projected effect on medical care, and organizational
factors reveal several barriers to successful guideline implementation
that should be addressed in the design of future guideline-based
interventions.

Despite the growing number of patients discharged from hospital with a

diagnosis of unstable angina, the diagnostic procedures and treatment
of unstable angina are still greatly debated, as they have been for
patients with myocardial infarction. In recent years the definition and
classification of the clinical syndrome of unstable angina has been
subjected to numerous proposals by distinguished cardiologists.

31 | P a g e
An attempt to clarify and redefine practical guidelines for different
subgroups of patients has been developed and carried out by the US
Agency for Health Care Policy and Research (AHCPR).

The current medical approach to treatment of patients with unstable

angina is discussed in detail, analysing the role of antiplatelet
medications, β-blockers, nitrates, heparin and calcium antagonists. The
small subgroup of patients with refractory unstable angina should
undergo urgent coronary angiography and revascularisation. Previous
and current research on medical treatment with thrombolytic therapy,
GPIIb/IIIa platelet receptor blockers and direct thrombin inhibitors is
outlined, keeping in mind one of the main aspects of pathophysiology of
the disease, that is ongoing thrombus formation.

In the future, a more aggressive strategy aimed at normalising the

atherogenic lipid profile in this very high risk group of patients should
be carried out, based on the positive results of lipid-lowering drug trials
both in primary and secondary prevention.

Upcoming research /study

Coronary angioplasty is known to mediate an inflammatory response.
Recently, we have characterized the transient systemic inflammatory
response after coronary stent implantation in patients with unstable
angina by measuring different soluble protein markers. In the present

32 | P a g e
study we have characterized the expression of various cellular activation
markers in neutrophils, monocytes and lymphocytes from the same
group of patients. Peripheral blood samples were taken before and 24 h,
48 h and 7 days after successful coronary stenting in 58 patients. Cell
surface markers (CD11b/CD18 and CD38) were analyzed by flow
cytometry to determine the activation of neutrophils, monocytes and T
lymphocytes. We found that coronary angioplasty with stent implantation
produces an increase in the cell surface expression of CD11b/CD18 in
neutrophils and CD38 in monocytes, following a similar time-course with
a peak after 24 h, returning to basal levels after 48 h and a second peak
after 7 days. However, T lymphocytes were not found to be activated.
These results suggest that coronary stent implantation induces a
different pattern inducing soluble and cellular inflammation markers, and
therefore, they should be taken into account in patients undergoing stent
implantation to study clinical correlations.

The initiating event in unstable angina (USA) and non-Q-

wave myocardial infarction (NQMI) is the rupture of an
atherosclerotic plaque resulting in local thrombosis. The
current standard treatment is the administration of aspirin
and heparin. The introduction of low-molecular-weight
heparin (LMWH) offers a potential alternative therapy.
Clinical mals have begun to examine the efficacy and
safety of using LMWH in the management of acute
coronary syndromes. Two pivotal studies have evaluated
the effects of LMWH preparations on patients with USA or
NQMI: The ESSENCE and the TIMI 11B trials. These studies
suggest that LMWH plus aspirin is more effective and
safer than unfractionated heparin in preventing myocardial
infarction, recurrent angina, or death. Because of these
differences, the American College of Cardiology and the
American Heart Association have updated their guidelines
for the treatment of USA and NQMI.

33 | P a g e
AKNOWLEDGEMENT
IN PREPARATION OF MY CASE STUDY, I HAD TO TAKE THE HELP
AND GUIDANCE OF SOME RESPECTED PERSON,WHO DESERVE
MY DEEPEST GRATITUDE. AS THE COMPLETION OF THIS CASE
STUDY GAVE ME MUCH PLEASURE, I would like to show my gratitude
Dr. paresh navlkar,LIHS for giving me good guideline for case study
throughout numerous consultations .I would also like to expand my
gratitude to all those who have directly and indirectly guided me in
writing this assignment .Many people ,especially my classmate and
family have made valuable comment suggestions on my paper which
gave me an inspiration to improve the quality bof the case study.

REFERENCE

34 | P a g e
35 | P a g e
36 | P a g e
37 | P a g e
38 | P a g e
39 | P a g e